The cellular biology of the human trabecular meshwork will be studied to gain insights into the pathogenesis and treatment of glaucoma. Studies will continue to use the perfusion organ culture system of the trabecular meshwork developed previously. This system allows trabecular cells to remain in situ on the trabecular lamellae and receive a flow of culture medium which flows through the meshwork in physiological fashion and enters Schlemm's canal. In an attempt to understand steroid glaucoma, the effect of dexamethasone on the glycosaminoglycans of the meshwork will be analyzed with microscale biochemical quantitation of individual meshworks. The time-dependent induction by dexamethasone of specific meshwork cellular and secreted proteins will be examined with SDS-PAGE. A computerized, automated, and continuous pressure monitoring system will record intraocular pressure and its potential elevation by the dexamethasone. The propensity for laser trabeculoplasty and fibroblastic growth factor to stimulate trabecular cell replication, as determined by 3H thymidine labelling, will examined. The effect of such cell replication on outflow facility will be determined. The short and long-term effect of potential aqueous outflow agents on meshwork histology and facility of outflow will be determined. These include epinephrine, ethacrynic acid, plasmin, and cytochalasin D. The effect of glaucoma surgery on the remaining meshwork will be studied, looking for evidence of "silting in" and the contribution of this to the syndrome of marked elevation of intraocular pressure after closure of a cyclodialysis cleft.